From Rindfliesch's discovery of the central vessel in the MS lesion in 1863, to CCSVI and the CNS lymphatic discovery. 160 years of research on blood flow, CSF, lymph and perfusion of the central nervous system.
Because the heart and the brain are connected.

Welcome! This blog contains research & information on lifestyle, nutrition and health for those with MS, as well as continuing information on the understanding of the endothelium and heart-brain connection. This blog is informative only--all medical decisions should be discussed with your own physicians.

The posts are searchable---simply type in your topic of interest in the search box at the top left.

Almost all of MS research is initiated and funded by pharmaceutical companies. This maintains the EAE mouse model and the auto-immune paradigm of MS, and continues the 20 billion dollar a year MS treatment industry. But as we learn more about slowed blood flow, gray matter atrophy, and environmental links to MS progression and disability--all things the current drugs do not address--we're discovering more about how to help those with MS.

To learn how this journey began, read my first post from August, 2009. Be well! Joan

Monday, March 20, 2017

In the name of research, and with a bit of curiosity, I tried a fast. I've recenly completed the ProLon Fast Mimicking Diet. More details about the specifics later, but first, you may well be asking---why would someone who LOVES food (yes, a lot link) voluntarily go on a five day fast? Believe me, I asked myself the same question.

Honestly, I wanted to check out the program before sharing more research with you all. I really think this is an interesting approach for MS, as it potentially reduces inflammation, boosts cellular rejuvenation, and resets the immune system. This program has had great success for patients with diabetes and cancer, as well. It's beginnings were in anti-aging therapies, and clinical trials in many chronic conditions related to aging are ongoing.

Fasting is not something people with MS should do without a doctor's supervision. I had to get approval from the ProLon nurse (over the phone) before starting the program---and I'm healthy. People with MS will need even further approval from their doctors, which is a really good thing. But it might be worth exploring. You can take the research and links to your doctor and see if this might be right for you. Jeff said he's interested after watching me last week, so we'll clear it with his doctor and do it together later this year.

Here's the science. In 2016, a study at the University of Southern California researched fasting and multiple sclerosis, and found that caloric reduction with a fast mimicking diet (FMD) did all sorts of wonderful things for the body, which specifically helped those with MS.

The USC study in mice with EAE and humans with MS found that a fast mimicking diet (FMD) made the body produce more of the hormone corticosterone, which in turn killed off damaging and inflammatory immune cells, and led to a production of new, healthy stem cells. This study also saw regeneration in myelin producing cells, and reduction of MS symptoms. All amazing stuff! Here's more on his study in layman's terms link Here is the complete paper, which I suggest reading, and sharing with your doctor if you're interested. Cell Reports FMD in MS publication

It's potentially an affordable alternative treatment for MS --so get ready for pharma to try and take it down with their own "trials" ( link to "Pragmatic Trial" of fasting with Tysabri ) You know something is worthwhile when pharma gets involved in debunking.

The lead USC researcher, Dr. Valter Longo, also discovered that fasting does not necessitate complete avoidance of food, but a fasting state can be reached by restricting caloric intake in a specific manner. Thus the "fast mimicking" part. This is something which might be easier for most of us to accomplish, and this was a key point for me. I could never do a liquid fast. I simply get too light headed and tired from low blood sugar. But I found this program to be much different, and very doable.

I'd had some nice back and forth e-mails with Dr. Longo when this research was first published last year. We both share a love of music and medicine. He was a young music student in Italy before coming to the states to study jazz guitar. He became interested in the study of aging, and got his PhD in biochemistry at UCLA, then joined the USC Davis School of Gerontology. He is also Director of the USC Longevity Institute. His focus is on how caloric restriction and fasting kills damaging cells while inducing healthy stem cell production. link to Dr. Longo's story

I had wondered if any of his FMD studies had looked at markers of inflammation related to endothelial improvements. I had found prior research looking at this connection. link He replied that his group wasn't looking at that specific aspect. He felt that the benefit of FMD was more about reduction of damaging autoimmune cells and a rejuvination of stem cells. But I have a hunch the increase in cortisone is also helping strengthen endothelial cells and reduce cell permeability--as well as helping the microbiome. The FMD has been shown to reduce C reactive protein in other studies, so there is a vascular connection. I hope more research will be done on these other aspects of the program.

Since I wanted to remain impartial in my analysis of Dr. Longo's FMD, I didn't ask him for a sample. I purchased the $300 ProLon FMD for myself online. (Still can't believe I shelled out big bucks to starve myself.) I hoped for benefit. I have some pain from a bit of osteoarthritis in two fingers and my neck, and lowering inflammation might help me. Losing weight wasn't my primary objective, but I figured it would be a nice side effect. I'm turning 55 this week, and my vanity continues. Jeff and I already follow the Endothelial Health Program. We eat whole, organic foods, mostly plants and no processed food, no dairy or gluten, so I was already in the right dietary zone. Just had to halve my daily caloric intake. Gulp.

The things I liked about ProLon were that it is a plant based and gluten free diet, shipped in a box right to my front door. It was very easy to follow. Each day had a separate carton, which was clearly labled with nutritional information and instructions. You can learn more about the specifics of this diet here: https://prolonfmd.com The reason it is a five day fast is because it takes that long for the body to reprogram and for cells to rejuvenate. Dr. Longo recommends doing this fast every three to four months. I think I could handle it a few times a year.

I believe it would be pretty easy to hack this program and do it on my own now. I have all of the caloric and nutrient info. But it's nice to have the supplements and energy drink and everything timed and packaged. Makes it easier to follow, and you're less likely to stray, when you think about how much you spent. The food was surprisingly palatable. I loved the kale crackers, and the instant soups were hearty and filling. The breakfast bar was nutty and satisfying to chew. Olives for snacks was fine with me. And the herbal teas were nice. I felt better knowing Dr. Longo is donating the proceeds to charity. He's a good guy. Anyone who studies jazz guitar and wants people healthier without drugs is OK in my book. link

How did I feel after 5 days of eating under 800 calories? It's odd, I wasn't really hungry, except for one day. I was surprisingly energized, and not fatigued. The hardest part of this program was giving up my usual three cups of caffeinated coffee a day. Prolon allows only one caffeinated drink per day, and this left me with a nasty caffeine withdrawal headache after day 1. However, I didn't feel sluggish without the coffee and I guess that must be from the cortisone coursing through my body. I was really hungry on day 3, and wanted to quit, but curiosity kept me going. That, and a bit of pride.

Jeff said he felt guilty eating in front of me. But he got over that and ate just fine! I also had to prepare a big dinner for some friends who happened to be in town on Day 2, and that was pretty hard. Standing over the stove, cooking and serving a delicious meal and then sitting and watching eveyone happily eating while I sipped herbal tea is not something I want to do again.

Now for the good stuff. I slept really well, and am still having very vivid, lucid dreams. I wake up ready to go, not groggy at all. And my skin looks great! It could be the fact I didn't had any alcohol, sugar or animal products for 5 days, but my eye bags are less noticeable and my complexion looks rosy. And my arthritis pain is much, much better. My knuckles are less stiff, and my neck has been feeling great. I was able to keep active, out walking, running errands and doing my normal routine, without feeling faint. I didn't have any recording or performing work during this week, so I could take it relatively easy. And I lost three pounds! Not as much as many others report (average loss is 5 lbs.) but hey, I'll take it.

Final thoughts. What we eat matters. Our bodies are miraculous machines, and it makes sense that the manner in which we fuel ourselves has repercussions on our health. By putting the body in a fasting state, we kick it into survival mode. We were created to withstand periods with limited caloric intake, and our body knows how to utilize our stored sugars and fats reserves. Most of us in the industrialized western nations eat much more than we need, far too many processed foods, too much animal protein and sugar, and not enough plants.

But this isn't to cast blame for being sick! No one gives themselves MS, cancer, osteoarthritis, or Alzheimer's. We don't control our genetic predispositions, and we all will die eventually. Here's Dr. Longo's TedX talk about how "if one disease doesn't get you, another one will!" He shows that it is possible to live longer, healthier lives. link There are things in our control which we can do to feel better, function better, and maybe even heal, including fasting. I believe the future will provide more understanding of our microbiome and brain, and how they are connected via the thousands of miles of lymph and blood vessels which keep our organs protected, nourished and cleansed. And a lot of that depends on food.

Also, as it is the Lenten season, I couldn't help but feel more meaning to the fast. Christians are taught to fast or give up something during Lent, to remind ourselves of Christ's forty days of fasting, praying and temptation in the desert before his eventual arrest and crucifixion. This is practiced, not as an exercise in self-denial, but in order to draw closer and more reliant on God. And for that reminder, I am thankful.

Wednesday, March 15, 2017

It is now quite obvious that Anthony Traboulsee meant what he said back in 2010. He does not believe the venous system has anything to do with Multiple Sclerosis, and that people with MS should not worry about their vascular health. They simply need to take their drugs.

This is in sharp contrast to peer-reviewed research conducted in labs around the globe; redefining the connection of the brain to the vasculature. link

Commenting on the failure of the UBC trial to prove any benefit in (under) treating stenotic veins, he gave patients the bright side. “Fortunately, there are a range of drug treatments for MS that have been proven, through rigorous studies, to be safe and effective at slowing the disease progression.”

Macleans Magazine journalist Anne Kingston questions why the UBC CCSVI trial released results before the study was actually completed. Read her well-researched article here: link
I think it's important to understand exactly why Tony needed to stop further exploration of the vascular connection to MS and state that the UBC study was the final word which debunked CCSVI research--- even though his study was not complete, and there are other placebo control CCSVI studies currently in Australia and Italy. He wants this research over. Tony's whole life, lab and career hinge on the maintenance of the EAE autoimmune model of MS, and the success of drugs. Especially one monoclonal antibody which targets the protein CD52 found on t and be cells, called Lemtrada.

Tony has been working hard for the Sanofi Genzyme Company for several years, as a saleman for Lemtrada. He is a paid researcher and spokeperson for Lemtrada. He has been touting this wonder drug around the world. Don't believe me? Behold, the google results of Traboulsee + Lemtrada.link

Genzyme Corp. paid out over 5 million dollars to US doctors from 2013-15 for promoting Lemtrada. This information is not available for Canada--but I believe we can assume that payments were equally high. link

Lemtrada is Dr. Traboulsee's "Top Pick" for his MS patients. Here's a blogger sharing this news.

Today is my 3rd MRI. I have a new neurologist.....Dr. Traboulsee also gave me some new options to check out, including his top pick called Lemtrada. Lemtrada sounds like an interesting choice, as it is administered one or twice a year. link

Tony believes that Lemtrada is the future of MS treatment.

But this isn't actually true. Lemtrada can't the future, because it's the past. It has a very well-documented research history since the mid 1900s, and has been used as an MS treatment since 1991, when it was called Campath.

Campath (alemtuzumab) was developed to treat B cell leukemia, but there were problems with that, so it was tried for immune suppression for organ transplants, and had a few too many side effects there, so it was tried in autoimmune diseases. It never became the big money maker drug companies had hoped for. It was first used as an off-label drug for multiple sclerosis in the UK.

The problem with using Lemtrada/Campath as an MS treatment was that it did not help people who were already progressive. In fact, as researchers were dismayed to find out, people with progressive MS disease worsened on the drug.“We realised that, although we had stopped disease activity in terms of new inflammatory brain lesions and had reduced the number of attacks that people were having, most of our patients were continuing to deteriorate.” The problems that the patients had when they started Campath-1H treatment were slowly progressing. This observation puzzled the researchers. If MS is an inflammatory autoimmune disease, why was Alemtuzumab treatment failing to help people in the progressive phase of the disease even though the treatment seemed to turn off inflammation?link

Unfortunately, this did not lead to a clinical improvement in the disability in these patients. In fact, their disability worsened with time at a rate of 0.02 EDSS points for each patient each year. Evidence for continued neurodegeneration in these patients was shown by progressive cerebral atrophy on follow-up MRI scanning. This particular group of patients who showed continuing disease progression had the highest inflammatory load prior to commencing alemtuzumab therapy. This group of patients were followed up with MRI scanning many years later (14 years post treatment) and did not demonstrate any increase in lesion load but did demonstrate further cerebral atrophy [Coles et al. 2006]. This was reflected in their EDSS score, the median being 7.5 (range 4.5–9) at latest follow up [Hill-Cawthorne et al. 2012].link

Campath 1H treatment was associated with a sustained and marked reduction in the volume of Gd enhancement, indicating suppression of active inflammation. Nevertheless, many patients developed increasing brain and spinal cord atrophy, T1 hypointensity, and disability. link

Disability in all but one of the 37 patients continued to worsen
progressively despite alemtuzumab treatment, as previously
reported.8 9 At the last recorded follow-up, a median of 14 years
post-treatment, the median disability estimated in 35/37
patients was EDSS 7.5 (range 4.5e9). Relapses were uncommon
but were not systematically captured. link

So, as you can see from these studies, to claim that Lemtrada slows progression or reverses MS is simply (excuse me) bullshit. What has changed? Campath has been renamed and rebranded. It's being given to a very specific population of people with MS. Lemtrada is helpful for people with highly inflammatory, brand new MS, because it wipes out the immune system and halts inflammation. As I've referred to this kind of immune ablation before--it's like "using a sledgehammer to swat a fly." This early intervention is being touted as a "window of opportunity."Treatment response to alemtuzumab is strongest as long as active inflammation is the predominant pathophysiological feature, and it is becoming less efficacious in neurodegeneration-dominated later stages of the disease. Thus, the optimal placement of alemtuzumab within treatment algorithms of MS is crucial. The impressive efficacy of alemtuzumab is counteracted by a less favorable safety profile. link

Tony knew how to get around that problem of MS progression. He only enrolled young people and people with early RRMS in his Lemtrada trial. And voila! Success! It's amazing what drugs can do when you get rid of those pesky older and progressive patients. He saved them for the CCSVI trial, where the median age was 50, and most were progressive.

Now that he’s managed a trial of 80 patients on Lemtrada (alemtuzumab), Traboulsee believes the future of MS is very treatable. Traboulsee believes he’s part of a movement that’s 10 years ahead of the curve and thinks this treatment might be resetting the immune system in patients who receive it. -link

What a trend setter Tony is with his deadly drug from the 1900s! It is because of Tony's work that Lemtrada became available in Canada in 2013. Tony's trials at UBC paved the way. Yet even with all of this hoopla in Canada, the FDA panel in the US was concerned about adverse effects and lack of evidence and decided not to approve Lemtrada.

They then voted almost unanimously that the sponsor had not provided sufficient evidence of a reduction in disability with alemtuzumab, but then subsequently decided that, assuming the efficacy results were as they appeared, safety results would not preclude approval. The panel also voted unanimously (with 2 abstentions) that if the drug were approved, it should not be indicated as a first-line agent in MS.link

The FDA panel mentioned the fact that Lemtrada had only been tested in young patients, those with a new MS diagnosis, and that the adverse effects of this drug were too risky. Like me, they read the prior research on Campath. They did not think it was an appropriate first line treatment for those newly diagnosed. And then, after pressure was put on the FDA by the National MS Society with some help from Genzyme, in a surprise turn-around ruling, Lemtrada was accepted by the FDA with black box warnings. Sadly, since 2013, we have a better understanding of the long-lasting side effects of Lemtrada.

Like a severe B-cell mediated disease of enhancing demyelination, which was caused by Lemtrada, and is even worse than just MS. link

or death from cancer, ITP and thyroid disease and a slew of other problems that come from destroying immune cells....Patients did have serious, even fatal, side effects while using Lemtrada, including viral infections and infusion reactions, and the drug may cause malignancies such as thyroid cancer, melanoma, and lymphoproliferative disorders. As a result, it is only available through a restricted distribution program, the Lemtrada REMS (Risk Evaluation and Mitigation Strategy), to ensure that patients prescribed Lemtrada are enrolled in the program and undergo periodic monitoring to detect potential health risks.

Which makes sense, when you consider the Kipnis Lab's recent discovery of a new lymphocyte which protects the gut and the brain. These type 2 lymphocytes are called "powerful defenders" and may be essential for the brain to heal after injury or an MS relapse. We have no idea on how destroying them with Lemtrada may affect long term health.link

Don't believe me? Let's hear from some of Tony's patients--- from public reviews.

I've had R-R MS for 18 years. I've been symptom free for 5 years. My previous MS Specialist, Dr.Hoogie retired and the doctor he referred me to was on mat leave when it was time for my annual check-up so I went to see him. He's well reputed as a researcher and is head of the MS Clinic at UBC, so I thought I was in good hands. I found out he is not what I want in a Doctor. He pushed his drug study on me really hard. I went home and researched the drug he's studying and it has caused death due to massive organ failure in one patient the UK. I don't have severe enough MS to want to try that kind of drug. When I asked him questions, he didn't really answer them clearly. I went back to my GP and asked for another referral to another MS Specialist. I strongly believe he should not be a practicing Doctor - he does it to pressure and try to recruit more patients for his studies and because he has to. I'm sure he's a good clinician and researcher. If you have a severe case and want to try to get access to what will be expensive, and hard core drugs that are not yet available to the public, go see him. But I don't want to be a lab rat.

+++++++++++

To begin, I was diagnosed with MS just over 18 years ago, a mere six months after graduating high school. Following a couple of weeks in the hospital, I was referred to the UBC MS Clinic and assigned to Traboulsee. He lied to me from the start, insisting there were no treatment options for the neuropathic pain and muscle spasms I suffered. Instead he claimed that there were only clinical trial studies and that he could do nothing more than sign me up to become a lab rat. Out of desperation, I enrolled on one clinical trial which saw me bed ridden from the side effects of that drig that was later proven to be useless for MS. When telling Traboulsee this during the trial, he ignored my severe reactions to the trial study drug and tried to convince me that I was actually doing better because of the experimental drug, though he should have been able to know that since the study was double-blinded. At one point I was able to procure a copy of my records from the clinic, only to find that Traboulsee had falsified many portions of my records, including one that indicated he had recommended various medications to me which I had refused. In reality, I had requested one type of medication for my MS symptoms which Traboulsee had refused me on the basis that he didn't like my attitude in not wanting to take part in further trial studies. Traboulsee should also set he watch as he is always an hour late for every appointment. He never answers any questions, is always reading the patient file, and ignore basic human rights.

++++++++++++

I believe that the behaviour of this Doctor is unacceptable, he was rude, condescending and at times devoid of any compassion or empathy. Moreover, he has extremely poor communication skills. I believe he is quite brilliant in his research, however, he should not be dealing with patients on a one on one basis. The sad part is he truly sees nothing wrong with his behaviour and can be vindictive and arrogant if you question what he has said. By not listening to his patients and showing them compassion he is doing a disservice to those looking to him for help.

++++++++++++

This doctor is horrible and a complete jerk. If you care about your health of that of a loved one you will seek medical expertise elsewhere. Nightmare treatment and responsible for the loss of my loved one. Only cares about research and treating patients as guinea pigs. Arrogant, condescending and doesn't care about human life or treatment - he only cares about MRIs and research not the person. Unsympathetic and a complete jackass of a person.

+++++++++++++++

Horrible. Saw him in summer, I have been so upset about his lack of care his and condescending tone that I am only now able to write this. Cares about money not about treating patients. Avoid this "doctor". He has to look things up on Google. Smug, wants you to join a clinical trial, otherwise dismisses you.

I have no idea where it leaves you, but I hate having to write about this man. I hate his arrogance, his lack of compassion, his lack of morals, ethics, and his tunnel vision. This is why I said I was walking away earlier this year...because I abhor these people and what they do to others, and it's upsetting.

But I keep writing and staying involved, because I love other people more. I was recently told by a commentor on this blog that I have no right to say anything about MS, because I do not have it. She said that I do not understand how it feels to have an incurable disease. And I agree with her. I have no idea. But I don't think that means I can't discuss new research, or walk alongside people with MS and encourage them. Nor do I think I need to say that there is no vascular connection to the MS disease process, when more and more peer-reviewed science continues to show this reality.

I've been going thru test results with a girlfriend this week. Her husband was just diagnosed with MS. She's asking for more blood panels, allergy tests, consulting with a vascular doctor and neurologist, and working with her GP. I'm going through all the various diet and lifestyle programs with her as her family comes to grips with this diagnosis. This week I also had a delicious seafood dinner overlooking the Pacific with another girlfriend who has MS, and she is thriving and healthy and amazing. I answer e-mails and phone calls, and try to encourage others. Because I live with proof of the importance of dealing with vascular health. I tell everyone, I AM NOT A DOCTOR. But I can read, and I can write. And I can encourage.

Jeff reminds me every single day that people with MS have more control than the Traboulsees of the world tell them. That the vascular connection is real. It may not be the complete picture, but it is part of the answer.

I hope there is an investigation into conflicts of interest with Dr. Traboulsee and the UBC Clinic.
If you have MS, and you love Lemtrada, and it's changed your life, no need to flame me. If you love Dr. Traboulsee. good for you! I'm happy for you! Honest! Be well, and continue in good health. My concern is that the UBC clinic is not looking at the big picture in MS treatments and manipulating research. And we all want the complete picture, right?

Thursday, March 2, 2017

I want to say upfront, I am not hopeful regarding the results of the University of British Columbia (UBC) CCSVI trial. The preliminary results may be most dramatically revealed at the Society of Interventional Radiologist conference on March 8th in the Marquis Ballroom of the Marriot in Washington DC. I have a pretty strong hunch they will be negative and will not show any benefit in venoplasty for CCSVI. I wish I could be more upbeat and say that this trial will give CCSVI venoplasty intervention a fair shot, but I've been concerned about bias and an ill-conceived trial since the beginning. Anne Kingston wrote the best article on this topic back in 2012--"Finally, CCSVI Clinical Trials. So Why is Everyone So Pissed Off?" linkHere is what I thought about Traboulsee's 2014 CCSVI imaging study- Scientific Misconduct?Fast forward to 2017. Even though the UBC CCSVI study is still on-going, preliminary results have been fast-tracked for a release at a vascular conference in the US. This research was submitted to the SIR conference after the deadline for submissions in September. This is from the SIR website, where the investigators are allowed to explain why their presentation deserves consideration. Please provide a justification below for this abstract's eligibility to be considered for late-breaking submission.

This will be the first presentation of a randomized, double blind clinical trial of jugular and azygos venoplasty in MS, including patient reported, clinical, and MRI outcomes. The presentation will include all data from the first 48 weeks in all patients after their first procedure only, comparing sham to venoplasty.

This is a multicenter trial with an independent trial coordinator. The database was locked December 23, 2016 and the authors were (and still are) blinded to the outcome. It is a trial of sufficient magnitude and scientific rigor that it deserves presentation at a major society meeting.link (search "Traboulsee" to see the submission)

Get that? The trial coordinators and authors claim to still be blinded to results. Seems odd, right? Why submit to SIR, a "major society meeting" without knowing the results? And why now? Why not wait until all the data has been collected and collated?I believe the reason the UBC study was submitted to SIR, before completion and after the SIR deadline, is because Dr. Zamboni announced, at the Veith Conference in November 2016, that his Brave Dreams Trial had been completed and results would be published in mid-2017. link

The UBC team submitted their abstract after Dr. Zamboni's announcement, as I believe they wanted to get out in front of the Brave Dreams published study results and put the final "nail in the coffin," ring the last "death knell", be the "last word" (or fill in any of the other hyperbolic titles for anti-CCSVI publications over the last five years.) I honestly think they want to kill this research and be done with it.

Joan, wait... (you say to me) this UBC study is gold-standard research! You sound like a conspiracy theorist. Science is science. Blinding and placebo controlled trials are what you have been asking for! This is exactly what the vascular connection to MS needs---independent study. That doesn't mean you get the results you want! Also, didn't you say you're done with all of this???

Yes, you're absolutely right. And I am done, but felt it was important to go on record. Here's my problem. This study does not look at blood flow before and after treatment. They did not measure venous pressure--so how could they possibly know if stenosis had been treated?The results of this study are not all objective. Dr. Zamboni has stated that the Brave Dreams trial results are objective. Objective results are numbers and stats and things that can be measured and tallied using unbiased machines. Venous pressure is an objective measure. Not questionaires from subjective humans compiled by even more subjective humans.

There was no retreatment for restenosis in the UBC trial (a problem for 50% of patients) or suggested aftercare and lifestyle intervention. Jeff had to be retreated at Stanford, as he developed intimal hyperplasia. He also had aftercare treatment and drastically changed his lifestyle, diet and exercise program.

Angioplasty for carotid artery stenosis has had placebo control trials, and you know what metric they used to measure success? Size of stenosis and blood flow. That's it. Not a questionaire asking "how are you feeling?" The researchers measured blood flow before and after and at monthly intervals up to a year. They used ultrasound to see how carotid stenosis looked, if there was restenosis it was re-treated. And most importantly, after treatment, they put the study participants on an aftercare program, making sure they had blood thinning treatment and that they exercised and ate better. Trial participants quit smoking or lost weight, if warranted. Because without aftercare and lifestyle changes, restenosis can be immediate, and all gains from angioplasty are lost. IRs know this.link

Take my husband's reversal of gray matter atrophy on MRI. No one can call that placebo! He doesn't just feel better or have less brain fog. His brain shows objective healing on MRI. He has had no new lesions, and his old ones have shrunk. Another objective measurement from Jeff's venoplasty treatment was blood flow. His jugular vein blood volume doubled after being stented. Other research has shown that CSF flow increased after treatment for CCSVI. linkThese are all benefits which can be measured using medical equipment, and are not part of the UBC data.

I fear the UBC researchers are going to say any subjective benefit after treatment is placebo. That there are no objective benefits in those treated, because they have not measured blood flow, CSF flow and gray matter atrophy. They certainly didn't retreat restenosis. And Charcot will be laughing, once again, at how easily he is able to control the mind of the hysteric, labile, desperate MS patient. link

4. Timing of release is suspicious
5. A history of bias and nay saying against CCSVI from trial lead investigator

Don't be discouraged. No matter what the UBC researchers claim, or how loudly they say it, it isn't over. Italy and Australia still have their trials. And we have other reseachers looking at the vascular connection. This research is not going away. Not with the ISNVD, not with The Gladstone Lab, The Kipnis Lab, the Nedergaard Lab and others--all committed to getting to the bottom of the vascular connection to diseases of neurodegeneration.

And I may be wrong!! Let's hope for that! Please let me be wrong!!!!
In the meantime, live your best, vascularly healthy life.
(Because I'm right about that part :-) )

About Me

I became interested in multiple sclerosis (MS) research when my husband Jeff was diagnosed with MS in 2007. I noted a connection of Jeff's disease process to his circulation and blood, and by accessing medical journals on the internet and stacks of books at my local library, I put together research to address this. I sent my theory and research, called the Endothelial Health Program, to universities, and began a correspondence with vascular specialists at Stanford University.
Jeff was the first American treated for CCSVI, and he is now eight years past his venoplasty, with no further MS progression, healing of his gray matter, and relief of many symptoms. He's still jogging, working full time as a composer and conductor, and traveling the globe.